The first phase of the study of peripheral arterial disease in the diabetic has been completed. A total of 707 study subjects have been recruited. These study subjects are currently being called to return to repeat studies as part of the research protocol. The following measurements have been collected at baseline and are currently being collected in year 03: systolic blood pressure at rest and after exercise in the upper and lower extremities utilizing transcutaneous Doppler techniques; measurement of pulse volume of the extremities by segmental plethysmography and Doppler examination of the arteries; fasting plasma glucose, serum cholesterol and triglycerides; quantitative lipoproteins; platelet factor 4; circulating platelet aggregates; platelet aggregation studies; ristocetin Willebrand factor and Willebrand antigen. Measurements of hemoglobin A1c and 2,3 diphosphoglycerate have been added to the study protocol for years 03 and 05. Initial clinical data have been abstracted on all subjects at the time of their return visit. At this time 358 patients have returned for repeat studies. The initial platelet survival studies have been carried out in 114 subjects: 27 normal subjects, 29 patients with occlusive arterial disease of the lower extremities without diabetes and 58 diabetic patients with and without occlusive arterial disease of the lower extremities. Repeat platelet survival studies are currently being scheduled and 27 such studies have been completed as of this date. The initial clinical and laboratory data have been collected, edited and corrected and entered into the master file. The same process is being carried out for the collection of the data in year 03. This study will provide information as to the natural history of the progression of vascular disease in diabetic patients and whether these changes can be correlated with plasma glucose, diabetic control (hemoglobin A1c), serum lipids, platelet and plasma coagulation factors and red cell 2,3 diphosphoglycerate. If such correlations exist, they may provide a mechanism for the development of atherosclerotic lesions in the diabetic and may point to the need for new modes of therapy.